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L0301P66 - Neurophysiology - Brain and Spinal Cord
__TOC__ Spinal Cord *nerves connect at every segment on both sides of the cord *grey matter **nerve cell bodies *white matter **dorsal columns - axons going up to and down from the brain Anatomy of the Spinal Cord Neural Pathways *sensory neurons pass through the dorsal root ganglion *motor neurons extend from the ventral part of the spinal cord to muscles *autonomic nerves pass through the sympathetic chain ganglion Sensory Input Nerve Fibres *A-α: **proprioceptors of skeletal muscle **thick diameter, low leakiness due to myelination - fast conduction *A-β: **mechanoreceptors of skin **myelinated *A-δ: **pain, temperature **constitute afferent portion of the reflex arc **myelinated **smallest of the A-type nerve fibres *C: **temperature, pain and itch **slow, long-lasting pain **non-myelinated - hence they are slow Termination *A-δ and C terminate early in the dorsal horn *while A-α and A-β terminate much deeper in the ventral area of the white matter Sensory Neuron *only if membrane potential still reaches threshold between the surface of skin to the myelinated area of the neuron, then APs be generated and transmitted to the spinal cord Sensory Pathways to the Brain Dorsal Column-Medial Lemniscal Pathway *involves the large sensory neurons (axons) for touch and proprioceptive information *cell body is in the dorsal root ganglion *signal sent up into the hindbrain by the axon in the dorsal column **stays on the same side as the side which the nerve entered the spinal cord *at the medulla, the axon crosses into the medial lemniscus (centre of the medulla) *transmitted to the thalamus of the brain then the sensory cortex Spinothalamic Pathway *involves the small sensory neurons (axons) for pain and temperature information *cell bodies also in the dorsal root ganglion *axon crosses the midline while in the spinal cord and ascends to the brain via the spinothalamic tract *no synapsing in the medulla occurs Spinal Reflexes *bypasses the brain for an immediate response Interneurons *located towards the midline of the spinal cord *provides essential Inhibition - automatic reciprocal action by antagonistic muscles *Reflex Arc - interneuron directly connects sensory neuron and motor neuron allowing for fast response while signal also sent to brain   Interneuron Activity *has its own spontaneous AP bursts Mechanism: *Glutamate **EPSPs, depolarisation and APs – Ca2+ influx via NMDA *Increase in cytoplasmic Ca2+ **activation of Ca2+ sensitive K channels (IKCa) **hyperpolarisation *Decrease in cytoplasmic Ca2+ **closing of KCa channels *allows better understanding of the nervous system which can be used to aid those with lack of muscular control Neuromuscular Junction *motor neuron extends from the ventral root of the spinal cord *large synapse per neuron at the centre of each muscle fibre **maximum surface area = max. reception of ACh and max. stimulation **therefore nearly always reaches threshold *transmitter: Acetylcholine (ACh) *metabolising enzyme: acetylcholinesterase *large ACh exocytosis and large receptor area = contraction always guaranteed Comparison: NMJ vs CNS Neurotransmission in CNS has: *variable transmitters *quantal release at most synapses *saturation of ionotropic receptors *astrocytes and removal *probability of release <1 *failures are often *synapse can be enhanced or suppressed *flexibility while NMJ does not. Nociception *sensory nervous system's response to certain harmful or potentially harmful stimuli *involves the A-δ and C nerve fibres *distinct pathway compared to that of mechanoreceptors Nociceptors *free, branching, unmyelinated nerve endings that signal that the body tissue is sign damage or is at risk of bring damaged *selective activation leads to conscious experience of pain 1. Information into the CNS:  C-Fibre Transmitters *two transmitters which are released simultaneously: *glutamate *substance P = protein Gate Theory of Pain *nociceptive signal is sent to brain via a projection neuron in the spinothalamic tract **allows one to feel the sense of pain *C fibre also synapses with an inhibitory interneuron **prevents too much pain reception from a relatively minor injury - foot on tack *large sensory fibres (mechanoreceptors), when stimulated, send off collaterals that activate inhibitory interneurons **often produce presynaptic inhibition on dorsal root nociceptor fibres thereby inhibiting transmission of pain *faults with this system = chronic pain Chronic Pain Occurs when there are problems with: *interneuron/projector neuron nociception *ion transporters Problem with the GABAa receptor *research: **activator isoguvacine generally causes hyperpolarisation, but occasionally causes depolarisation instead **blocker bicuculline blocks both **∴ the receptor is GABAa *faults with Cl- concentration = action potentials are produced when they aren’t meant to *when normal: **Cl- is low inside cell ***channels opens and Cl- enters **potassium-chorine (KCC) pump ensures Cl- is low in cell *But it can be damaged during traumatic brain injury or hypoxic stress, therefore when faulty: **when NKCC1 is more dominant thus Cl- is too high in the cell **when channels open Cl- moves out of cell causing depolarisation (membrane becomes less negative) **thus an inhibitory neuron becomes an excitatory neuron 2. Pain in the Brain *afferent information goes to the thalamus via the spinothalamic tract *thalamus in turn sends it to the: **sensory cortex ***allows sensation of pain **prefrontal cortex via anterior cingulate cortex ***controls cognition and behaviour **amygdala via ínsula ***controls aggression and defence *this is the reason why those with chronic pain experience other problems including emotional dependencies, cognition issues *causes many changes including: **white matter integrity in these regions ***↓ fractional anisotropy (FA) **reduction in opioids (involved in hyperpolarisation) and thus opioid receptor binding **grey matter health ***↓neuronal marker N-acetyl aspartate (NAA) **enhances neuroinflammation 3. Brain Modulation of Spinal Reflexes *information transmission back down to the spinal cord from the brain *involves the enkephalin interneuron Enkephalin Interneurons *enkephalin - body’s own opioids *found in the dorsal horn *only activated after the brain is notified of the pain in order to protects your body from feeling too much pain Process *releases its opioids which bind to opiate receptors which are metabotropic *results in the inhibition of EPSPs: *presynaptically by hyperpolarisation and postsynaptically Referred Pain *when one to feel pain at a site other than source of pain *occurs when: **nociceptive fibres from 2 areas enter the dorsal horn at the same level **more specifically: low-use sensory inputs (viscera) synapse at same spinal level as high-use inputs (skin) **causes the brain to confuse noxious stimulus as coming from the high-input nerve and thus feel pain *do not have pain receptors: **heart and appendix **thus heart conditions and appendicitis cause pain in the surrounding area Botox *in small amounts can be very beneficial *prevent docking process in synaptic transmission *maybe used to diminish chronic pain in the future if injected in the correct area